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Lupus/Rheumatoid Arthritis (Auto Immune Disorders) Research Directory

Magnesium deficiency in systematic Iupus erythematosus

Subject(s): MAGNESUM deficiency diseases; SYSTEMC lupus
erythematosus -- Diagnosis
Source: Journal of Nutritional & Environmental Medicine, Jun97, Vol. 7
ssue 2, p107, 5p, 1 chart
Author(s): Romano, Thomas J.
Abstract: Discusses the effects of reduced erythrocyte magnesium
(Mg) deficiency in patients with systematic lupus erythematosus (SLE).
Common symptom of the disorder; How to determine if SLE patients are
also prone to hypomagnesemia; Results of the study.
AN: 9711141130
SSN: 1359-0847
Full Text Word Count: 2470
Database: Academic Search Elite
Reduced erythrocyte magnesium (Mg) levels have been reported in fibromyalgia syndrome (FS), chronic
fatigue syndrome (CFS), myofascial pain syndrome (MPS) and eosinophilia myalgia syndrome (EMS).
These disorders have chronic pain as a common symptom. Chronic pain also affects some patients with
systemic lupus erythematosus (SLE). To determine if SLE patients are also prone to hypomagnesemia,
red blood cell (RBC) and plasma Mg levels were measured in all SLE patients seen in a general
rheumatology practice in a 3-year period. There were 25 such patients with a mean age of 47 years.
Thirteen SLE patients had FS and 12 did not have either FS or MPS. The mean RBC Mg level for the
SLE patients was 4.60 mg dl-1, statistically significantly lower than that of the reference controls and 12
osteoarthritis controls. t did not matter whether the SLE patients had ES or MPS. This finding has
implications for diagnosis and treatment.
Keywords: magnesium, myaIgias, Iupus, pain.
Reduced erythrocyte magnesium (Mg) levels have been reported in fibromyalgia syndrome (FS) [ 1],
chronic fatigue syndrome (CFS) [ 2], myofascial pain syndrome (MPS) [ 3] and eosinophilia myalgia
syndrome (EMS) [ 4]. These four disorders have chronic pain and/or fatigue as a common denominator.
Furthermore, it has been proposed that low Mg levels predispose patients to myalgias [ 5] and that low
muscle Mg levels correspond to a low pain threshold [ 6]. Systemic lupus erythematosus (SLE) is also a
condition that can be characterized by chronic pain in some patients. Lupus patients have often been
described as having myalgias, arthralgias and pain resulting from inflammation of such structures as the
lung pleura and/or pericardium [ 7-9]. f patients experience pain because of a flare of this systemic
inflammatory connective tissue disease the treatment would typically be medications such as
glucocorticosteroids or even immunosuppressants [ 10, 11]. However, if low Mg is causing or contributing
to increased pain in SLE patients without any concomitant increase in inflammatory activity, the use of
these medications would not be expected to ease the pain and could perhaps be counterproductive
because of side-effects. With this in mind the Mg levels were checked in SLE patients in a general
rheumatology practice.

During the period September 1992 to May 1995 inclusive, 25 SLE patients were evaluated and treated in
a general rheumatology practice. All the patients fulfilled 1982 American College of Rheumatology (ACR)
criteria for SLE [ 12]. There were four males and 21 females with a mean age of 47 years (range 18-64
years). Thirteen SLE patients (one male and 12 females) fulfilled the ACR criteria for FS [ 13]. The
remaining 12 patients (three males and nine females) had neither FS nor MPS.
During the study period, none of the SLE patients exhibited renal insufficiency nor was there evidence of
myositis. None of the SLE patients had creatine phosphokinase (CPK) or aldolase levels outside of the
'normal range'. The mean CPK level for all 25 patients was 126 U 1-1 (normal range 32-236 U 1-1). The
mean aldolase level for the eight SLE patients tested was 4.8 U 1[sup -1 (normal range 1-8 U 1-1). As a
control group, 12 patients with uncomplicated monoarticular osteoarthritis (OA) (four hip, six knee and two
shoulder) were also studied. There were three men (ages 44, 48 and 53 years) and nine women (mean
age 50 years and range 42-64 years) in the OA group (see Table 1). None of the OA or SLE patients was
taking diuretics or uricosuric drugs. None was bulimic, anorexic or using laxatives inappropriately. No
patient was cachetic or on a 'crash' diet at the time of the study. None was taking vitamin supplements. All
had simultaneous plasma and red blood cell (RBC) Mg determinations.
All 25 SLE patients had venous blood drawn for both RBC and plasma Mg levels. The samples were
drawn into a heparinized tube from a peripheral vein. They were immediately refrigerated and then
transported to a reference laboratory (National Medical Services, Willow Grove, PA, USA) where the
assays were performed. The plasma and RBC Mg levels using washed cells were determined by using
direction dilution techniques and atomic absorption [ 14, 15] and the results here reported in mg dl-1.
The mean RBC Mg level for the SLE patients without FS or MPS was 4.50 mg dl-1 with a standard
deviation of 0.72 mg dl-1 whereas the mean RBC Mg level for the SLE patients with FS was 4.63 mg dl-1
with a standard deviation of 0.68 mg dl-1. There was no statistically significant difference between these
two groups. The mean RBC Mg level for all the SLE patients was 4.60 mg dl-1 with a standard deviation
of 0.70 mg dl-1, which is statistically significantly different from that of the reference controls (5.5 mg dl-1
and standard deviation 0.65 mg dl-1) and 12 osteoarthritis controls (5.30 mg dl-1 and standard deviation
0.62 mg dl-1). A comparison of the means tests showed a z score of 4.60 and p < 0.001. The plasma Mg
levels for the SLE patients were not significantly different from the reference controls and also the
osteoarthritis controls. The mean plasma Mg level for the SLE patients was 2.00 mg dl-1, which is not
statistically significantly different from the mean plasma Mg level for the reference controls and for the 12
osteoarthritis controls (2.05 and 2.00 mg dl-1, respectively).
CIinicaI Vignette
A 35-year-old white female with a history of SLE for 9 years presented with a 3-month history of gradually
increasing myalgias. There was no change in diet or exercise nor was she taking any new medications.
Her SLE had been well controlled on prednisone (5 mg/day) and azathioprine (150 mg/day). She required
occasional prescriptions for non-steroidal anti-inflammatory medications such as Salsalate of up to 3
g/day for arthralgias. On physical examination the patient had normal blood pressure. An examination of
the head, ears, eyes, nose and throat was unrevealing. n particular, there was no alopecia, oral ulcers or
malar rash. A cardiopulmonary examination was unremarkable. An abdominal examination was benign. A
musculoskeletal examination revealed no signs of synovitis, bony ankylosis or joint effusions. There was
fairly good range of motion of all the joints: however, there was some diffuse tenderness on palpation of

the muscles. There were only four of 18 fibromyalgia tender points noted (bilateral trapezius, right second
rib and left gluteus medius). She did not fulfil the ACR criteria [ 13] for FS. Laboratory values revealed
normal renal function and normal levels of sodium, potassium, chloride and bicarbonate. Her erythrocyte
sedimentation rate (ESR) was normal (10 mm). Her CPK and aldolase were also within the normal range
(164 and 4.0 U 1-1, respectively). However, her RBC Mg level was noted to be 3.8 mg dl-1 (reference
mean 5.5 mg dl-1 with a range of 4.2-6.8 mg dl-1). Her plasma Mg level was 1.7 mg dl-1 (reference mean
2.05 mg dl-1 with a range of 1.6-2.5 mg dl-1). The patient's dose of prednisone was not increased nor
was there a change in the dose or type of immunosuppressant. Rather, she was treated with six weekly
injections of magnesium sulphate (1 g intramuscularly) as had been described previously in the treatment
of CFS [ 2]. After the first series of six injections the patient's RBC Mg level increased to 4.3 mg dl-1,
barely within the normal reference range. However, the patient's myalgias improved significantly but did
not completely subside. t was not until a second course of six weekly injections of magnesium sulphate
(1 g intramuscularly) that the patient's myalgias almost disappeared. Her RBC Mg level increased to 5.4
mg dl-1. The patient was treated continuously with an oral magnesium supplement (magnesium chloride
(Slow- Mag) 64 ma, one tablet, three times a day with food). The subsequent RBC Mg level 6 months after
the initiation of the oral magnesium supplementation was 5.2 mg dl-1. The patient remains free of
As in the case of other painful conditions [ 1-3], statistically significant differences in Mg levels between
SLE patients and controls tended to be seen much more readily using RBC Mg levels as the measure of
total body Mg stores as opposed to the plasma Mg level. Most clinicians tend to use either serum or
plasma Mg levels and in doing so may overlook Mg deficiency in some patients, a potentially reversible
problem. t can be very dangerous to treat symptoms such as myalgias in SLE patients with an increase
of corticosteroids and/or immunosuppressants without checking the RBC Mg level first. f an SLE patient's
myalgias are due to a flare of this inflammatory connective tissue disease, it is certainly prudent to treat
with medication geared towards controlling the inflammation. However, if the patient's myalgias are due to
Mg deficiency, treatment with an increased dose of corticosteroids would likely be ineffective. n fact, the
literature suggests that corticosteroid treatment may even intensify the Mg deficiency [ 16-21]. t could
also cause complications such as avascular necrosis of the bone [ 22], osteoporosis [ 23], a hastening of
the development of cataracts [ 24] and other side-effects [ 25]. The use of immunosuppressants is also
not without risk. They can cause bone marrow suppression [ 26], liver toxicity [ 27] and other side-effects [
28]. These potential problems may be acceptable if one is treating a flare of SLE. However, if the
myalgias are due to hypomagnesemia, an increase in corticosteroids and/or a modification of
immunosuppressants therapy could expose the patient to needless risk.
Since the pain threshold tends to decrease as the total Mg levels decrease [ 5], it seems only reasonable
to check for hypomagnesemia in patients with an unexplained increase in chronic pain. This includes SLE
patients whose myalgias may be due to different causes on different occasions. Oral Mg products
suitable for supplementation are available over the counter, are relatively inexpensive and the Mg levels
can be monitored to avoid potential toxicity particularly in those SLE patients with renal insufficiency.
t is not known why Mg levels tend to drop in patients with chronic pain problems such as FS, MPS, EMS
and SLE. t has been suggested [ 3] that there may be a problem with Mg availability and/or utilization at
the tissue level as opposed to a suboptimal dietary intake or an increased excretion of Mg. Whatever the
mechanism, Mg deficiency should not go unnoticed. To fail to consider Mg deficiency in the differential
diagnosis of neuromuscular problems in SLE might expose such patients to undue risk and expense
particularly if myalgias are mistakenly attributed to inflammation.
TABLE 1. IndividuaI RBC determination (mg dI-1)
SLE patients (n 25) OA controls (n 12)(a)

- 6.8
- 6.2
5.6 -
5.4. 5.4 5.4, 5.4
5.3 5.3(c)
5.2 5.2
5.1 5.1
5.0 -
4.9, 4.9, 4.9 4.9
4.8, 4.8 4.8
4.7, 4.7 4.7
4.6, 4.6, 4.6(b) 4.6
4.5 -
4.3 -
4.0 -
3.9 -
3.8 -
3.0 -
3.0 -
2.8 -
(a) Twelve osteoarthrities patients with monoarticular disease.
(b) Mean = 4.6 mg dl-1 and standard deviation = 0.65 mg dl-1.
(c) Mean = 5.3 mg dl-1 and standard deviation = 0.62 mg dl-1.
Reference range mean = 5.5 mg dl-1.
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Source: Journal of Nutritional & Environmental Medicine, Jun97, Vol. 7
ssue 2, p107, 5p
tem: 9711141130
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